Heart Sounds
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Cardiovascular diseases continue to be the leading cause of morbidity and mortality worldwide. One of the first steps in evaluating the cardiovascular system after detailed history taking is physical examination. Auscultation of the heart forms the core of cardiac physical examination. Despite significant interobserver variability and need for habituation and training, cardiac auscultation provides important initial clues in patient evaluation and serves as a guide for further diagnostic testing.
Some of the common mechanisms by which heart sounds are generated include (1) opening or closure of the heart valves, (2) flow of blood through the valve orifice, (3) flow of blood into the ventricular chambers, and (4) rubbing of cardiac surfaces.
The main anatomic areas to focus on while initially evaluating heart sounds include the cardiac apex, the aortic area (second intercostal space [ICS] just to the right of the sternum or the third ICS just to the left of sternum), the pulmonary area (second ICS just to the left of sternum) and the tricuspid area (fourth and fifth ICS just to the left of sternum). [1] In addition, auscultation of the left axilla, base of the heart, carotid arteries, and interscapular area should be performed to assess for radiation of heart sounds and murmurs.
The patient should be examined in the supine position, in the left lateral decubitus position, and while sitting and leaning forward. Each area should be systematically auscultated for S1, S2, physiologic splitting, respiratory variations, and any accessory sounds during systole and diastole. [2] Whenever possible, auscultation should be accompanied by having the patient perform dynamic maneuvers such as standing, Valsalva, squatting, and hand grip, although these maneuvers are falling out of favor with the use of echocardiography.
While interpreting the heart sounds, it is essential to understand from which part of the cardiac cycle they are being generated. This can be done by palpating the carotid artery simultaneously while auscultating the heart. The carotid upstroke corresponds to ventricular systole.
The first heart sound (S1) is produced by vibrations generated by closure of the mitral (M1) and tricuspid valves (T1). [3] It corresponds to the end of diastole and beginning of ventricular systole and precedes the upstroke of carotid pulsation. Refer to the audio example below.
M1 is best heard over the apex of the heart, and T1 is best heard over the fourth ICS at the left sternal border.
Typically, S1 is a high-pitched sound best heard with the diaphragm of the stethoscope. The intensity of S1 depends on the integrity and pliability of valvular cusps, the length of the PR interval (which governs the velocity of valve closure), the strength of ventricular contraction, the presence or absence of valvular stenosis or regurgitation, the position of the valve leaflets at end-diastole, and the amount of tissue between the heart and the stethoscope. The role of these factors is discussed as below. [1, 4, 5]
The pliability of the valve cusps governs the ease of valvular apposition and closure. With an increased degree of calcification and fibrosis, pliability is lost, leading to diminished valvular mobility and diminished S1. This can happen in advanced rheumatic mitral stenosis (MS) and postradiation MS.
S1 is influenced by ventricular contractility. Positive inotropic forces lead to a rapid rise in ventricular pressure and a loud S1. A sharp rise in ventricular pressure causes more rapid increase in ventricular pressure relative to atrial pressure and a faster closure of atrioventricular (AV) valves, leading to louder S1. Similarly, negative inotropic forces lead to a diminished rate of rise in ventricular pressure and a diminished S1.
The PR interval governs the time that atria have to empty their contents into the ventricle. With a short PR interval, the atria have less time to empty into the ventricle, which leads to more forceful atrial contraction and maximal separation of the AV valves, leading to louder S1 upon valvular closure. In addition, the tachycardia associated with a short PR interval leads to a faster rise of ventricular systolic pressure relative to atrial pressure, with forceful closure of the AV valves and a loud S1. Similarly if the PR interval is prolonged, the atria have time to slowly empty into the ventricles, and the AV valves are less separated by the end of atrial contraction, leading to less forceful closure of AV valves and a lower intensity S1.
The valvular position at the end of ventricular diastole also determines the intensity of S1. The farther apart the leaflets are at the beginning of systole, the more rapid is their closure and the louder is S1. Similarly, the closer the leaflets are to each other at the beginning of the systole, the shorter the distance of travel required for valvular apposition and the softer the S1. The leaflets are far apart with increased transvalvular gradient (ie, MS or tricuspid stenosis [TS]), increased transvalvular flow (ie, with left-to-right intracardiac shunts at the level of the ductus or ventricle), tachycardia, and preexcitation syndromes.
With AV valvular regurgitation, the leaflets are not able to appose properly, leading to a muffled S1. In acute aortic regurgitation (AR), left ventricular (LV) end-diastolic pressure rapidly rises; thus, there is faster equilibration of ventricular and atrial pressures, leading to early closure of mitral valve and a muffled S1.
The S1 is muffled when there is an increased amount of tissue between the heart and the stethoscope, as occurs with pleural effusion, pericardial effusion, emphysema, pneumothorax, and obesity. Similarly, in thin-walled individuals, the heart is closer to the chest wall, and the sounds are better transmitted to the stethoscope, leading to a louder S1.
Conditions associated with a loud S1 include the following:
Increased transvalvular gradient (MS, TS, atrial myxoma)
Increased force of ventricular contraction (tachycardia, hyperdynamic states [ie, anemia, fever, thyrotoxicosis, exercise, inotropic agents])
Shortened PR interval – Tachycardia, preexcitation syndromes (ie, Wolff-Parkinson-White [WPW] syndrome)
Mitral valve prolapse (MVP), thin individuals
S1 can have a variable intensity in conditions that produce variable PR interval or variable ventricular contractility. This can happen in Mobitz type I heart block, digitalis toxicity, atrial fibrillation, and ventricular tachycardia with AV dissociation.
Conditions associated with diminished intensity of S1 include the following:
Inappropriate apposition of the AV valves (ie, mitral regurgitation [MR], tricuspid regurgitation [TR], dilated cardiomyopathy)
Prolonged PR interval (ie, bradycardia, heart block, digitalis toxicity)
Decreased force of ventricular contraction (ie, cardiomyopathy, myocarditis, myxedema, myocardial infarction [MI])
Increased calcification of the AV valve (ie, calcific MS, postirradiation)
Increased distance from the heart (ie, obesity, emphysema, pleural effusion, pericardial effusion)
Normally, the mitral valve closes just prior to the tricuspid valve. Thus, M1 is audible before T1 (a difference that is often not detectable).
Splitting of S1 is more prominent when the time difference between the closure of the mitral and the tricuspid valves is increased. This can happen with early closure of the mitral valve or a delayed closure of the tricuspid valve relative to the mitral valve.
Some of the conditions associated with a split S1 include the following:
Premature ventricular contractions (PVCs) of LV origin
Right bundle branch block
LV pacing
Ebstein anomaly
Atrial septal defect (ASD)
Additionally, in severe TS, the tricuspid valve closes after the mitral valve; this difference can be perceived on auscultation.
Reverse splitting of S1 occurs when M1 follows the closure of T1. This happens when the closure of mitral valve is delayed as can happen with left bundle branch block, right ventricular (RV) pacing, severe MS, and left atrial myxoma.
The second heart sound (S2) is produced by the closure of the aortic (A2) and the pulmonary valves (P2) at the end of systole. [6] Refer to the audio example below.
A2 is best heard at the aortic area (second right intercostal space); P2 is best heard at the pulmonary area. S2 is a high-pitched sound heard best with the diaphragm of the stethoscope. The intensity depends on valvular factors, the transvalvular gradient, mechanical factors, and size of the great vessels.
The intensity of A2 is increased with systemic hypertension, in coarctation of the aorta, in aortic aneurysm, in thin individuals, and when the aorta is closer to the anterior chest wall as may occur with tetralogy of Fallot and transposition of the great arteries (TGA).
Theintensity of A2 is decreased with decreased aortic diastolic pressure (as in AR), with improper valvular apposition (as can occur with AR or aortic dissection), calcific immobile valves (as may occur with calcific aortic stenosis [AS]), and decreased systemic arterial pressure.
The intensity of P2 is increased with pulmonary arterial hypertension [7] from any etiology. A loud P2 is also audible with ASD, [8] although the exact mechanism in this condition remains unclear.
Normally, the aortic valve closes slightly before the pulmonary valve. This difference is more pronounced with inspiration due to increased RV stroke volume.
S2 splitting results from the aortic valve closing slightly before the pulmonary valve, and this is more prominent with inspiration. The pulmonary and the aortic valves remain open briefly after the end of systole and after the LV and RV pressures have been lowered compared to aortic pressures. This interval between the actual valve closure and pressure crossover between ventricles and great vessels has been called the hangout time. [1] , which is inversely proportional to the resistance to blood flow in the great vessels. The pulmonary vascular resistance is less than the systemic vascular resistance. Thus, the hangout time is longer for the pulmonic valve than for the aortic valve. This accounts for delayed closure of pulmonary valve relative to the aortic valve.
With inspiration, pulmonary arterial resistance further declines, leading to further delay in pulmonary valve closure and a more pronounced split. [9] Another factor contributing to the delayed closure of pulmonary valve with inspiration is prolonged RV emptying time due to increased stroke volume as a result of increased preload with inspiration.
Wide S2 splitting
Normally, with expiration, S2 is single, as the aortic and the pulmonary valve closures occur almost simultaneously. If, at expiration, the two different components of S2 can still be appreciated separately, then S2 is said to be widely split.
The wide split can result from delayed closure of the pulmonary valve or early closure of the aortic valve during expiration.
Delayed closure of pulmonary valve can result from conduction or hemodynamic abnormalities. Delayed electrical activation of the RV accounts for a delayed onset of systole, with delayed completion of RV emptying and thus delayed closure of the pulmonary valve. This can happen with right bundle branch block, LV pacing, PVCs arising from the left ventricle, and WPW with preexcitation of the left ventricle. Hemodynamic reasons for delayed closure of the pulmonary valve include RV outflow obstruction (pulmonary valvular, supravalvular, or subvalvular stenosis), pulmonary hypertension, and pulmonary artery branch stenosis.
Early closure of the aortic valve occurs with early emptying of the left ventricle, as can happen with MR or with ventricular septal defect (VSD) with left–to-right shunting.
With widening of the S2 split, the respiratory variability is preserved (ie, with inspiration, the split becomes wider compared to expiration).
Wide fixed splitting
The split S2 is said to be widely fixed when the respiratory variability in the relation of A2 -P2 is lost and the time interval between A2 and P2 remains relatively constant, with P2 following A2. This occurs most commonly ASD with left-to-right shunting but can also occur with right ventricular failure.
The exact mechanism of the fixed-split S2 in ASD is unknown, but it is postulated that the RV systolic time remains relatively constant (ie, there is a loss of respiratory variability in RV stroke volume). In the presence of ASD with left-to-right shunt, the RV stroke volume is composed of contributions from the superior vena cava (SVC) and the left atrium. During inspiration, the contribution from the SVC is increased owing to increased blood flow from the body to the heart. During expiration, there is a greater flow across the atrial shunt. Thus, the net RV stroke volume remains constant throughout the respiratory cycle.
Conditions associated with RV failure may also cause fixed splitting of S2 by compromising the ability of RV to alter its stroke volume with respiration. This can occur with primary RV failure, pulmonary hypertension, and RV outflow tract obstruction.
Reverse splitting
When the A2 is audible after P2 during expiration, S2 is said to be paradoxically split. This can happen when the RV contraction is completed before LV contraction. This can result from conduction or hemodynamic reasons.
Reverse splitting due to conductive disturbance occurs in conditions that cause delayed activation (and thus delayed emptying) of the left ventricle, such as left bundle branch block, RV pacing, PVCs of RV origin, and preexcitation of the RV in WPW syndrome.
Reverse splitting due to hemodynamic reasons may occur with delayed emptying of the LV, as can occur with LV outflow tract obstruction caused by AS.
The third heart sound (S3) is a low-pitched, early diastolic sound audible during the rapid entry of blood from the atrium to the ventricle. When arising from the LV, it is best audible at the apex with the patient in left lateral decubitus position with breath held at end expiration. When it is of RV origin, S3 is best audible at the left lower sternal border or the xiphoid with the patient in supine position. These are best heard with the bell of the stethoscope. Refer to the audio example below.
The exact mechanism of genesis of S3 is debatable. Some of the proposed mechanisms are listed below. [10, 11, 12]
S3 occurs when rapidly rushing blood flow from the atria is suddenly decelerated by the ventricle when it reaches its elastic limit. In a normal ventricle, this can happen with excessive volume of incoming blood, as can happen in hyperdynamic states or volume-loaded conditions. Similarly, in a ventricle that is already stretched and overfilled owing to systolic dysfunction, even a relatively normal (or less than normal) amount of blood entry can stretch the ventricle enough for it to reach its elastic limit. With decreased compliance of the ventricle, as can happen with hypertrophy and diastolic dysfunction, a normal amount of blood entry during diastole can challenge ventricular elasticity and generate the S3.
Movement of ventricle closer to the chest wall (the so-called “impact theory”): When the ventricle is dilated, it moves closer to the chest wall. This close proximity of the ventricle to the chest wall leads to a more forceful impact with entry of blood during diastole.
S3 can be physiologically present in patients younger than 40 years. These patients often have a thin chest wall to permit the easy transmission of S3. In the presence of heart failure, S3 is a bad prognostic sign. [13] Conditions associated with pathological S3 include the following:
Systolic and/or diastolic ventricular dysfunction
Ischemic heart disease
Hyperkinetic states – Anemia, fever, pregnancy, thyrotoxicosis, AV fistula
MR or TR
Chronic AR with systolic dysfunction
Systemic and pulmonary hypertension
Acute aortic regurgitation
Volume overload – Renal failure
The fourth heart sound (S4) is a late diastolic sound that corresponds to late ventricular filling through active atrial contraction. It is a low-intensity sound heard best with the bell of the stethoscope. When of LV origin, S4 is best heard at the apex with the patient in the left lateral decubitus position at end expiration. When of RV origin, it is heard best at the left lower sternal border. Maneuvers that increase the preload increase the intensity of S4 by increasing the separation of S4 from S1. Left-sided S4 is also augmented by increased afterload as can happen with hand grip. Refer to the audio example below.
The exact mechanism of S4 generation is debatable. The ventricular theory proposes that S4 is generated by sudden deceleration of the jet of blood as it enters a ventricle with decreased compliance. The impact theory proposes the movement and impact of the ventricle on the chest wall as the jet of blood from atrial systole strikes the ventricle. In either case, active atrial contraction is necessary for the generation of S4. Thus, S4 is not audible with atrial fibrillation or flutter.
Some of the conditions associated with S4 include the following:
Ventricular hypertrophy – LV hypertrophy (systemic hypertension, hypertrophic cardiomyopathy, AS) [14] ; RV hypertrophy (pulmonary hypertension, pulmonary stenosis [PS])
Ischemic heart disease – Acute MI, [15] angina
Ventricular aneurysm
Hyperkinetic states that cause forceful atrial contraction
Both S3 and S4 need to be differentiated from splitting of the normal heart sounds. With splitting, the heart sounds are high pitched and best audible with the diaphragm, whereas the S3 or S4 are low-pitched sounds best audible with the bell of the stethoscope.
The opening snap (OS) is a high-pitched diastolic sound produced by rapid opening of the mitral valve in MS or tricuspid valve in TS. [16] When mitral in origin, it is best heard at the apex following the aortic sound A2, with the patient in left lateral decubitus position.
The time difference between the A2 and OS has a diagnostic implication. The closer the OS is to A2, the more severe the stenosis. The OS signifies the time moment when the left atrial pressure exceeds the LV diastolic pressure and marks the beginning of blood entry into the LV from the LA. The more severe the stenosis, the greater the LA pressure and the lesser the LA-LV early diastolic pressure gradient, leading to an early opening of the respective valve. In general, the relation between A2 and the OS depends on LV pressure at A2 closure, LA pressure at A2 closure, and the rate of LV pressure decline. [17]
The A2 -OS interval can be increased despite severe MS in patients who have systemic hypertension with an early closure of AV.
TS usually occurs in association with MS, and, as such, the findings are generally obscured by the findings of MS.
The ejection systolic sounds are heard during the early part of ventricular systole. These sounds are generally high pitched and best audible with the diaphragm of the stethoscope. They can be valvular or vascular in origin.
These are the systolic sounds that are audible in patients with defects in aortic or pulmonary valves. They are present in early systole after the S1. The aortic ejection sound is best audible at the apex or the aortic area. The pulmonary valve ejection sound is best audible at the pulmonary area.
The aortic valvular ejection sound is associated with bicuspid aortic valves and aortic regurgitation. Pliable valves generate a higher-intensity ejection click. The intensity of the ejection click decreases with increased valvular calcification. Thus, the aortic ejection click may be absent in severe calcific AS. [18] The ejection click is also absent in supravalvular or subvalvular AS. The presence of an aortic ejection sound, in the absence of other signs of AS, strongly suggests the presence of a bicuspid aortic valve. [19]
The pulmonary valvular ejection sound is predominantly associated with pulmonary valvular stenosis. [20] Unlike most right-sided sounds, the ejection click of PS is decreased in intensity with inspiration. One of the proposed mechanisms is a rapid opening of the valve from the closed position with expiration, giving rise to the high-intensity sound. With inspiration, the rapid jet from the right atrium can partially open the pulmonary valve during diastole; thus, the opening of pulmonary valve with the onset of RV systole is more gradual, leading to decreased intensity of the sound.
These sounds are produced at the aorta or pulmonary artery.
The aortic vascular ejection sounds are associated with aortic sclerosis with tortuous aortic root, systemic hypertension, ascending aortic aneurysm, and aortic root dilatation. This sound is usually audible at the aortic area and is not well transmitted to the apex.
The pulmonary vascular ejection sound is associated with pulmonary hypertension and pulmonary arterial dilatation. It is best audible at the left second and third intercostal area.
This is associated with mitral or tricuspid valve prolapse. Of the two entities, MVP is more common. Refer to the audio example below.
The mid-systolic click from mitral valve prolapse. Audio courtesy of 3M™ Littmann® Stethoscopes. (MP3)
The nonejection systolic click is a high-pitched systolic sound that follows S1 and is heard best at the apex (MVP) or the tricuspid area (tricuspid valve prolapse) with the diaphragm of the stethoscope. The interval between S1 and the prolapse click may vary depending on the volume status of the respective ventricles, as the prolapse occurs at a specific ventricular volume. [21] . Thus, if the end-diastolic volume of the ventricle is increased, as can happen with bradycardia, in the supine position, or during hand grip or squatting, the S1 -prolapse interval is increased.
Similarly, if the end-diastolic volume is decreased, as can occur in tachycardia, upon standing up, and during the Valsalva maneuver, the S1 -click interval decreases. This time-based variation can help identify the click of mitral or tricuspid prolapse from other heart sounds.
The production of murmurs results from turbulent flow across valves. Three main factors have been attributed to cause a murmur: (1) high flow rate through normal or abnormal orifices, (2) forward flow through a constricted or irregular orifice or into a dilated vessel or chamber, and (3) backward or regurgitant flow through an incompetent valve. [22, 1, 23]
When evaluating a heart murmur, it is important to know the timing of the murmur in the cardiac cycle, the location, the duration, character, configuration, radiation, aggravating maneuvers, and diminishing maneuvers.
Recognizing the periodicity of murmur helps to narrow the differential diagnoses and often guides further diagnostic evaluation. For example, all diastolic murmurs and any systolic murmur above grade 2 in severity requires further evaluation with echocardiography. [22] The timing of the murmur is determined by palpating the carotid pulse while listening to the murmur. The carotid upstroke corresponds to the onset of systole.
The factors to focus on while evaluating a murmur are discussed briefly below.
Intensity: The intensity of the murmur depends on the volume of blood flow across the valve and the pressure gradient across which the blood flow occurs. The intensity is graded into 6 different grades, as follows:
Grade I – Heard in a quiet room by an expert examiner
Grade II – Heard by most examiners
Grade III – Loud murmur without thrill
Grade IV – Loud murmur with a thrill
Grade V – Thrill with a very loud murmur audible with stethoscope placed lightly over the chest
Grade VI – Thrill with a very loud murmur audible even with the stethoscope slightly away from the chest
The grade of the murmur is important, as any diastolic murmur and a systolic murmur above grade II/VI in severity warrants echocardiographic evaluation as per ACC/AHA guidelines.
Timing: Depending on when they are best heard in the cardiac cycle, the murmurs can be systolic (holosystolic, early/middle/late systolic), diastolic (early/middle/late) or continuous (ie, present in both systole and diastole).
Location: This is the area of the heart where the murmur is heard the loudest. While auscultating, one should concentrate on the apex, pulmonary area, tricuspid, and aortic areas, in addition to the axilla, base of the heart, and left fourth ICS for evidence of radiation of murmur.
As shown in Table 3, the location and timing help in determining whether the murmur is arising from the right or the left side of the heart. In addition, the position can help in locating the involved valves.
Quality/character: Different murmurs have different qualities, such as harsh, blowing, rumbling, musical, or cooing. See Table 3.
Pitch: This can be high or low pitched depending on the frequency of the murmur. The high-pitched sounds are best audible with a diaphragm and the low-pitched sounds with the bell.
Radiation: Murmurs tend to radiate to certain specific areas that are often characteristic of a particular murmur. The murmur of MR radiates to the axilla or base of the heart, depending on which leaflet is involved. In the case of AS, the murmur radiates in the direction of the jet of turbulent blood (ie, radiates to the carotids). Similarly, the aortic regurgitant murmur tends to radiate along the left sternal border.
Configuration: This corresponds to the shape of murmur intensity over time. It can be a plateau, decrescendo, crescendo-decrescendo, or crescendo murmur.
Dynamic auscultation involves certain specific maneuvers that affect the blood flow through the valves and can aid in recognition and differentiation of heart murmurs.
Inspiration: Inspiration leads to a decrease in the intrathoracic pressure with an increase in venous return to the right side of the heart. The murmurs generated from the right side of the heart increase in intensity with inspiration.
Expiration: Expiration has the opposite effect as inspiration. There is an increase in the intrathoracic pressure and a decrease in venous return to the right side of the heart. Blood in the lung is “forced” into the left heart. Hence, murmurs arising from the left side of the heart become more prominent with expiration.
Standing up: This causes a peripheral pooling of blood and a net decrease in venous return. Most murmurs are thus decreased in intensity upon standing, except that of hypertrophic obstructive cardiomyopathy (HOCM) and MVP, which become more prominent.
Squatting: Squatting causes an increase in the afterload and venous return (ie, preload). The net effect is an increase in intensity of all the murmurs, except those associated with MVP and HOCM, which become less prominent with squatting.
Straight leg raising: Passive straight leg raising increases venous return (ie, preload) and has an effect similar to brisk squatting. All murmurs increase in intensity except those of HOCM and MVP, which decrease in intensity with this maneuver.
Hand grip: Hand grip is a form of isometric exercise and increases the afterload, arterial pressure, LV volume, and LV pressure. The net effect of these changes is complex and variable. Murmurs of MR, AR, and VSD worsen with hand grip, while those of HOCM and MVP become less prominent.
Valsalva maneuver: Valsalva maneuver involves asking the patient to strain, which increases the intrathoracic pressure, thus causing a net decrease in preload. Most heart murmurs decrease in intensity with Valsalva, except those of HOCM and MVP, which become more prominent.
Amyl nitrate inhalation: Amyl nitrate is an arteriolar vasodilator and initially causes decreased afterload followed by reflex tachycardia. During the initial phase, because of reduced afterload, the murmurs of AR, MR, and VSD diminish, while those of AS are accentuated. Later on, during the tachycardic phase, the murmur of MS is accentuated.
Table 1. Effect of Different Maneuvers on Some Common Murmurs (Open Table in a new window)
Murmur Type
Inspiration
Expiration
Passive Leg Raising
Squatting
Standing
Hand Grip
Valsalva
Amyl Nitrate Inhalation
TS
↑
↓
↑
↑
↓
↑
↓
↑
MS
↓
↑
↑
↓
↓
↑
↓
↓
MR
↓
↑
↑
↑
↓
↑
↓
↓
MVP
↓
↑
↓
↑/↓a
↑
↓
↑
↑b
AS
↓
↑
↑
↑/↓
↓
↓
↓
↑
AR
↓
↑
↑
↑
↓
↑
↓
↓
HOCM
↓
↑
↓
↓
↑
↓
↑
↑
VSD
↑↓
↑↓
↑↓
↑
↓
↑
—
↑↓
a With squatting, there is an increase in afterload and preload. Initially, the MVP click is delayed and murmur shortened, but, as the regurgitation worsens, the murmur may increase in intensity.
b The murmur and the click of MVP occurs earlier with amyl nitrate inhalation.
TS: tricuspid stenosis; MS: mitral stenosis; MR: mitral regurgitation; MVP: mitral valve prolapse; AS: aortic stenosis; AR: aortic regurgitation; HOCM: hypertrophic obstructive cardiomyopathy; VSD: ventricular septal defect
Table 2. Differential Diagnoses of Cardiac Murmur [29] (Open Table in a new window)
Systolic Murmurs
Early systolic murmur
Mitral – Acute MR
Tricuspid – TR
VSD – Muscular or non-restrictive with pulmonary hypertension
Mid-systolic/mid-to-late systolic murmurs
Aortic
Obstructive
Supravalvular – Supravalvular AS, aortic coarctation
Valvular – AS, aortic sclerosis
Subvalvular – HOCM
Increased flow, hyperkinetic states, aortic regurgitation, complete heart block
Dilatation of the ascending aorta, aortitis, atheroma
Pulmonary
Obstructive
Supravalvular – Pulmonary artery stenosis
Valvular – Pulmonary valve stenosis
Subvalvular – Infundibular stenosis
Increased flow, hyperkinetic states, left-to-right shunt
Dilation of the pulmonary artery
Late systolic murmurs
Mitral – MVP
Tricuspid – Tricuspid valve prolapse
Holosystolic murmurs
AV valve regurgitation – MR, TR
VSD with left-to-right shunt
Diastolic Murmurs
Early diastolic murmur
Aortic regurgitation
Valvular – Congenital (bicuspid valve), rheumatic, endocarditis, prolapse, trauma, postvalvulotomy
Dilatation of the valve annulus – Aortic dissection, annuloaortic ectasia, cystic medial degeneration, hypertension, ankylosing spondylitis, syphilis, Takayasu
Pulmonary regurgitation
Valvular – Postvalvulotomy, endocarditis, rheumatic fever, carcinoid
Dilatation of the valve annulus – Pulmonary hypertension, Marfan syndrome, Takayasu
Congenital – Isolated or associated with tetralogy of Fallot, VSD, pulmonic stenosis
Mid-diastolic murmur
Mitral
Mitral stenosis
Carey Coombs murmur (mid-diastolic apical murmur in acute rheumatic fever due to mitral valvulitis)
Increased flow across nonstenotic mitral valve (eg, MR, VSD, PDA, high-output state, complete heart block)
Tricuspid
TS
Increased flow across nonstenotic tricuspid valve (eg, TR, ASD, anomalous pulmonary venous return)
Left and right atrial tumors – Myxoma
Severe or eccentric AR (Austin Flint murmur)
Late diastolic murmur
Presystolic accentuation of MS murmur
Austin Flint murmur of severe or eccentric AR
Continuous Murmurs
PDA
Coronary arteriovenous fistula
Ruptured sinus of Valsalva aneurysm
Aortopulmonary window
Cervical venous hum
Anomalous left coronary artery from the pulmonary artery
Mammary souffle of pregnancy
Bronchial collateral circulation
Intercostal or pulmonary arteriovenous fistula
Systolic murmurs occur during the ventricular contraction. They can result from (1) leakage across the abnormal atrioventricular valves (tricuspid or mitral) or interventricular septal defects or (2) ventricular outflow tract obstruction, which can be valvular, supravalvular, or subvalvular. In some cases, the systolic murmurs can be audible owing to an abnormal amount of blood flow across normal valves, as can occur in hyperdynamic states.
Systolic murmurs can be holosystolic, early systolic, late systolic, or mid-systolic in their timing. As per the ACC/AHA guidelines, any patient with a holosystolic, early systolic, late systolic, or a mid-systolic murmur greater than II/VI in severity or with evidence of cardiac compromise due to valvular disease should be further evaluated with echocardiography. [22]
Early systolic murmurs
Early systolic murmurs are produced by acute MR or TR or in VSD with pulmonary hypertension. They are blowing in nature and decrescendo in character. Blood flows rapidly from the ventricle into an unprepared atrium, leading to rapid equalization of the pressures and early systolic murmur.
Acute MR can occur in the setting of an acute MI, infective endocarditis, chordal rupture in patients with MVP, or blunt chest wall trauma. In the acute setting, the LA does not have sufficient time to dilate in response to the high-volume regurgitant jet. Thus, the LA and LV pressures equalize in the early part of systole, confining the murmur to early systole. When acute, the murmur of MR is accompanied by an S4. MI can damage the papillary muscles, resulting in acute MR. This usually occurs on day 2-7 post–acute MI, and the posteromedial muscle is involved more often than the anterolateral muscle.
The murmur of acute MR must be differentiated from a murmur of ventricular septal rupture, which is usually holosystolic and associated with a palpable systolic thrill. Nevertheless, any newly onset systolic murmur following MI should be evaluated with echocardiography.
Infective endocarditis can directly damage the valve leaflets, the chordae, or both, producing MR. Blunt chest wall trauma can damage the papillary muscle and/or cause chordal rupture or valvular leaflet avulsion, leading to acute MR. Chordal rupture due to myxomatous degeneration caused by MVP or other associated connective tissue disease worsens the severity of a pre-existing murmur.
A small muscular VSD alone and a large VSD with pulmonary hypertension can also produce an early systolic murmur. These murmurs are soft and blowing and audible at the left lower sternal border. In case of a muscular VSD, the septal defect closes during septal contraction in systole, thus limiting the murmur to the early part of systole. In the presence of pulmonary hypertension with VSD, the pressure gradient is maintained between the left and the right ventricle only in the early part of systole. This confines the murmur to early systole.
Acute TR can occur in the setting of infective endocarditis. The murmur is usually soft, blowing, and decrescendo and is not associated with signs of right heart failure. It is often accompanied by a right-sided S4 and a diastolic flow rumble.
Mid to late systolic murmurs
These murmurs are usually associated with ventricular outflow tract obstruction (which can be valvular, supravalvular, or subvalvular) or an abnormal amount of blood flow across normal valves as can happen in hyperdynamic states (hyperthyroidism, fever, pregnancy, anemia, renal failure).
The murmur associated with valvular stenosis (AS or PS) is usually a harsh murmur which is crescendo- decrescendo in configuration and high pitched.
AS-associated murmurs are most audible at the right upper sternal border/right third ICS with the patient in the upright position and breath held at end expiration. In some cases, it is audible at the apex, in which case it can be confused with the murmur of MR. Some of the findings that help delineate the murmur of MR from that of AS include an audible S1, forceful apex, radiation to carotids, changes with atrial fibrillation, and post-PVC accentuation. The AS murmur usually radiates to the carotid arteries.
An S4 is audible with severe AS. The time to peak of murmur often depends on the severity of valvular obstruction. The later the murmur peak, the more severe the obstruction. The exact location of the murmur varies depending on whether the murmur is valvular, subvalvular, or supravalvular. A valvular murmur is most prominent at the right second ICS, while a supravalvular stenosis produces a murmur that is located slightly higher than the valvular murmur. Refer to the audio example below.
The murmur of PS is best audible at the left second ICS just to the left of sternum. It is late peaking, is crescendo-decrescendo in configuration, and may be associated with a systolic click that becomes softer with inspiration. The P2 is usually soft and S2 usually split, with the split directly proportional to the degree of stenosis. The split depends on the severity of the murmur. As the severity increases, the P2 component of the S2 is delayed to the extent that a severe stenotic murmur can overshadow the sound generated by aortic valve closure. In severe PS, a right-sided S4 is often audible.
The murmur of HOCM is most audible at the left lower sternal border, left fourth ICS. It is harsh and crescendo-decrescendo in character. The murmur of HOCM is dynamic, and its intensity varies with the changes in left ventricular outflow tract (LVOT). An increase in LV volume leads to a decrease in the severity of outflow tract obstruction, thus leading to a decrease in the intensity of HOCM murmur. This can happen during leg raising, during squatting, or with handgrip. Similarly, any decrease in the LV volume leads to an increase in outflow tract obstruction, increasing the intensity of HOCM murmur. This can be seen with Valsalva maneuver and sudden standing.
MVP produces a mid- to late systolic murmur that is preceded by a nonejection click. [24] The murmur is blowing and high pitched in nature. The murmur is increased in intensity upon sudden standing and Valsalva. Squatting, hand grip, and bradycardia decrease the intensity of MVP murmur.
Holosystolic murmurs
These murmurs last throughout ventricular systole. They usually start at S1 and proceed through S2; the intensity of the murmur may overshadow both valve closure sounds.
These murmurs are typically produced by emptying of the high-pressure ventricle during systole into chambers that have lower pressure at that time (the atria with MR or TR or the right ventricle in the case of VSD).
At the start of isovolumetric ventricular contraction, the ventricular pressure rapidly exceeds the atrial pressure. The abnormal AV valves cannot prevent the regurgitation of blood from ventricle to atrium. As a result, the high-pressure ventricle empties into the low pressure atria. This marks the beginning of the holosystolic murmur, in which the sound of murmur onset often muffles S1. The regurgitant murmur can also muffle S2, as the ventricular pressure continues to exceed atrial pressure for a short period after closure of the aortic/pulmonary valve.
The murmur of MR is blowing and high pitched and is best heard at the apex with radiation to the axilla or the base of the heart. It is usually plateau in configuration. The MR murmur is increased during expiration, passive leg raising, squatting, and handgrip and decreased in intensity with inspiration, Valsalva, and standing. The radiation of the murmur depends on which leaflet is involved. A murmur generated by the deformity of anterior leaflet radiates more toward the axilla, thoracic spine, and scapula, while a murmur arising from posterior leaflet involvement radiates to the base of the heart. [25]
The presence of S3 with valvular MR indicates a more severe and hemodynamically significant lesion. The association of signs of pulmonary hypertension and right heart failure also indicate hemodynamically significant MR. Refer to the audio example below.
The murmur of TR is best heard at the left lower sternal border. It is a blowing high-pitched murmur heard that increases in intensity with inspiration (Carvallo sign). It can result primarily from involvement of the tricuspid valve or secondarily from pulmonary hypertension. When due to pulmonary hypertension, it is associated with a loud P2.
In VSD with normal pulmonary arterial pressures, a holosystolic murmur can be heard over the left lower sternal border at the level of the third and fourth ICSs. This murmur depends on the orifice size of the septal defect. The smaller the defect, the greater the intensity of the murmur.
With a larger orifice size, RV and pulmonary pressure increase, confining the murmur to early systole. Subsequently, once pressure equalization occurs, blood flow is absent. This is associated with pulmonary hypertension and is a bad prognostic sign, as it indicates progression of disease. Thus, the presence of holosystolic murmur in VSD indicates early disease and, depending on clinical setting, carries a better prognosis than the absence of a murmur in the presence of VSD. Refer to the audio example below.
Innocent murmurs and functional systolic ejection murmurs
Innocent murmurs are mid- to late-systolic, medium- to high-pitched ejection murmurs audible at the left lower sternal border or the left second ICS, depending on origin from the LV or RV outflow tract. These murmurs are usually blowing in character and grade I or II/VI in intensity. They can vary in intensity with the body’s positioning and always end before the closure of the semilunar valves. Murmurs are categorized as innocent only if examination of the cardiovascular system reveals normal findings.
Functional systolic ejection murmurs are associated with increased blood flow across the semilunar valves (aortic/pulmonary). Some of the conditions associated with functional murmurs include anemia, thyrotoxicosis, pregnancy, fever, exercise, arteriovenous fistula, and complete heart block. With complete heart block, there is beat-to-beat variation in the murmur intensity.
Diastolic murmurs are audible during ventricular diastole and caused by either (1) regurgitation across the aortic or pulmonary valve or (2) stenotic AV valves.
Early diastolic murmurs
Early diastolic murmurs are produced by either AR or pulmonary regurgitation.
The AR murmur is a soft high-pitched sound, is decrescendo in configuration, and is most audible at the left sternal border or the right second ICS just to the right of sternum, with the patient leaning forward at end expiration. The murmur radiates to the left lower sternal border if it is due to primary valve disease. In patients with aortic root disease, the murmur may radiate to the right sternal border. The murmur increases in intensity during expiration and decreases in intensity with hand grip, squatting, Valsalva, and amyl nitrate inhalation. The S2 is usually muffled with AR, and there is an audible wide physiologic split. Refer to the audio example below.
The murmur of pulmonary regurgitation is best audible at the pulmonary area. The character, quality, and pitch of the murmur vary depending on the presence or absence of pulmonary hypertension. In the presence of pulmonary hypertension, it is a high-pitched, decrescendo murmur also known as a Graham Steell murmur. S2 is usually loud in association with pulmonary regurgitation. In the absence of pulmonary hypertension, it is a low-pitched crescendo-decrescendo murmur.
Mid- to late diastolic murmurs
These murmurs are produced by the blood flow across stenotic AV valves.
MS produces a low-pitched, mid-diastolic, rumbling murmur with presystolic accentuation, best heard with the bell of the stethoscope placed over the cardiac apex with the patient in the left lateral position. S1 is loud. The murmur usually follows an OS, and the interval between the A2 and OS is inversely proportional to the severity of obstruction.
The murmur of MS is increased in intensity with expiration and maneuvers that increase cardiac output, such as exercise. The presystolic accentuation results from atrial contraction in late diastole and is absent in patients with atrial fibrillation. The duration of murmur corresponds to the period in which the LA-LV diastolic pressure gradient is maintained. This duration correlates with the severity of obstruction; the longer the murmur duration, the more severe the MS (provided the diastolic filling time is not shortened, as may happen in tachycardia).
The duration of murmur does not correlate to the severity of MS in high-output states, such as pregnancy, as the murmur is long-lasting owing to increased blood flow. Similarly, in the presence of pulmonary hypertension or right heart failure, the flow across the mitral valve is decreased, and, even in severe MS, the duration of murmur may be shortened. Refer to the audio example below.
TS produces a low-pitched, mid-systolic rumbling murmur best audible at the left third ICS/left sternal border and xiphoid process. The murmur increases in intensity with inspiration (Carvallo sign) and decreases in intensity during expiration and with Valsalva maneuver.
Atrial myxoma can produce a diastolic murmur that is very similar to that associated with MS or TS. This murmur is also low pitched, mid-diastolic, and rumbling with presystolic accentuation. An OS is absent and is replaced by a “tumor plop.” It is difficult to clinically differentiate the murmur of atrial myxoma from that of MS, but the murmur of atrial tumors changes in intensity as the patient changes positions.
Austin Flint murmur: This is an early diastolic rumbling murmur associated with valvular AR. This murmur arises from aortic regurgitant jets abutting the LV free wall and causing premature closure of the MV. [26] The Austin Flint murmur decreases in intensity with maneuvers that would decrease the intensity of AR, such as afterload reduction with amyl nitrate. On the other hand, amyl nitrate inhalation would increase the intensity of MS. This can potentially differentiate Austin Flint murmur from MS murmur.
Carey Coombs murmur: This is a mid-diastolic murmur audible during acute rheumatic fever over the apical impulse. It is attributed to acute mitral valvulitis due to rheumatic fever.
States of increased flow across AV valves can also produce diastolic rumbling murmurs. Patients with MR have an increased amount of diastolic blood flow across the mitral valve. There is a partial closure of the mitral valve in mid diastole after wide opening of the valve leaflets during early diastole. This, combined with increased blood flow, causes a functional MS murmur. [27] Similarly, ASD with left-to-right shunt can produce a mid-diastolic rumbling murmur over the tricuspid area.
These murmurs are audible in systole and diastole, although their intensity usually varies during systole and diastole. They result from a communication between a high-pressure arterial and low-pressure venous chamber or vessel. Some of the causes of continuous murmurs are listed in Table 2.
The continuous murmurs produced by patent ductus arteriosus (PDA) result from an abnormal communication between the aorta and the pulmonary artery. The aortic pressure is always higher than that of the pulmonary artery and results in a continuous murmur, with peak flow occurring during the end of systole (ie, at S2). The murmur is blowing, high pitched, and best audible at the left upper sternal border near the left second ICS.
If the communication is large, pulmonary arterial pressure eventually rises, leading to pulmonary hypertension. This may cause the diastolic component of the murmur to become muffled; in severe pulmonary hypertension, it may lead to reversal of flow during diastole and differential cyanosis. The continuous murmur of PDA may be confused with the murmur associated with AS with coexisting AR. In the case of AS with AR, the murmur is least intense around S2, while, in PDA, the murmur is most pronounced at S2.
The continuous murmur from anomalous origin of left coronary artery from the pulmonary artery (so called Bland-Garland-White syndrome) can produce a continuous murmur best audible around the left sternal border. In this case, the collateral vessels from the right coronary artery to the left coronary artery give rise to the continuous murmur. Rupture of a sinus of Valsalva into the RA or RV can produce a continuous murmur best audible over the lower left sternal border and the xiphoid. These murmurs are more pronounced during diastole, a fact that differentiates them from the murmur of PDA.
Coronary artery fistulas emptying in the RA can produce a continuous murmur audible at the right or left sternal area. These murmurs are more prominent in diastole, as the flow in the coronary arteries occurs during diastole.
A continuous murmur due to coarctation of aorta is best audible at the level of coarctation, usually between the shoulder blades.
Table 3. Summary of Characteristics of Some Common Murmurs (Open Table in a new window)
Murmur Type
Location
Quality
Periodicity
Configuration
Radiation
S1
S2
Pitch
MS
Apex
Rumbling
Diastolic
Mid to late diastolic with presystolic accentuation
—
Loud
Initially normal; later, loud P2 with pulmonary hypertension, ultimately single S2
Low
MR
Apex
Blowing
Systolic
Plateau
Axilla/base of heart
Muffled
Widely split
High
AS
Apex/right upper sternal border
Harsh
Systolic
Crescendo-decrescendo
Carotids
Normal
Delayed aortic valve closure causing narrow split or single S2
High
AR
Right upper sternal border/left third/fourth ICS
Blowing
Diastolic
Decrescendo
Apex
Normal/soft
Soft A2, P2 may be obscured by murmur
TR
Left fourth ICS
Blowing
Diastolic
Plateau
Left sternal border/over xiphoid
Muffled
When TR is due to pulmonary hypertension, P2 is accentuated with delayed split
High
PS
Left second ICS
Blowing
Systolic
Crescendo/decrescendo
—
Normal
Loud P2 with prominent split, which becomes fixed with increasing severity
High
VSD
Left lower sternal border
Harsh
Systolic
Plateau
None
—
Split
High
PDA
Left upper sternal border
Harsh
Continuous
Crescendo-decrescendo with peak around S2
None
Normal
Widely split S2 due to delayed P2
High
MVP
Apex
Blowing
Mid-late systolic
Plateau
Axilla/base
Diastolic click
After S1
—
High
HOCM
Left lower sternal border
Harsh
Mid-late systolic
Similar to valvular AS murmur
None
Normal
Normal initially, with increased severity; S2 paradoxically split
High
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Murmur Type
Inspiration
Expiration
Passive Leg Raising
Squatting
Standing
Hand Grip
Valsalva
Amyl Nitrate Inhalation
TS
↑
↓
↑
↑
↓
↑
↓
↑
MS
↓
↑
↑
↓
↓
↑
↓
↓
MR
↓
↑
↑
↑
↓
↑
↓
↓
MVP
↓
↑
↓
↑/↓a
↑
↓
↑
↑b
AS
↓
↑
↑
↑/↓
↓
↓
↓
↑
AR
↓
↑
↑
↑
↓
↑
↓
↓
HOCM
↓
↑
↓
↓
↑
↓
↑
↑
VSD
↑↓
↑↓
↑↓
↑
↓
↑
—
↑↓
a With squatting, there is an increase in afterload and preload. Initially, the MVP click is delayed and murmur shortened, but, as the regurgitation worsens, the murmur may increase in intensity.
b The murmur and the click of MVP occurs earlier with amyl nitrate inhalation.
TS: tricuspid stenosis; MS: mitral stenosis; MR: mitral regurgitation; MVP: mitral valve prolapse; AS: aortic stenosis; AR: aortic regurgitation; HOCM: hypertrophic obstructive cardiomyopathy; VSD: ventricular septal defect
Systolic Murmurs
Early systolic murmur
Mitral – Acute MR
Tricuspid – TR
VSD – Muscular or non-restrictive with pulmonary hypertension
Mid-systolic/mid-to-late systolic murmurs
Aortic
Obstructive
Supravalvular – Supravalvular AS, aortic coarctation
Valvular – AS, aortic sclerosis
Subvalvular – HOCM
Increased flow, hyperkinetic states, aortic regurgitation, complete heart block
Dilatation of the ascending aorta, aortitis, atheroma
Pulmonary
Obstructive
Supravalvular – Pulmonary artery stenosis
Valvular – Pulmonary valve stenosis
Subvalvular – Infundibular stenosis
Increased flow, hyperkinetic states, left-to-right shunt
Dilation of the pulmonary artery
Late systolic murmurs
Mitral – MVP
Tricuspid – Tricuspid valve prolapse
Holosystolic murmurs
AV valve regurgitation – MR, TR
VSD with left-to-right shunt
Diastolic Murmurs
Early diastolic murmur
Aortic regurgitation
Valvular – Congenital (bicuspid valve), rheumatic, endocarditis, prolapse, trauma, postvalvulotomy
Dilatation of the valve annulus – Aortic dissection, annuloaortic ectasia, cystic medial degeneration, hypertension, ankylosing spondylitis, syphilis, Takayasu
Pulmonary regurgitation
Valvular – Postvalvulotomy, endocarditis, rheumatic fever, carcinoid
Dilatation of the valve annulus – Pulmonary hypertension, Marfan syndrome, Takayasu
Congenital – Isolated or associated with tetralogy of Fallot, VSD, pulmonic stenosis
Mid-diastolic murmur
Mitral
Mitral stenosis
Carey Coombs murmur (mid-diastolic apical murmur in acute rheumatic fever due to mitral valvulitis)
Increased flow across nonstenotic mitral valve (eg, MR, VSD, PDA, high-output state, complete heart block)
Tricuspid
TS
Increased flow across nonstenotic tricuspid valve (eg, TR, ASD, anomalous pulmonary venous return)
Left and right atrial tumors – Myxoma
Severe or eccentric AR (Austin Flint murmur)
Late diastolic murmur
Presystolic accentuation of MS murmur
Austin Flint murmur of severe or eccentric AR
Continuous Murmurs
PDA
Coronary arteriovenous fistula
Ruptured sinus of Valsalva aneurysm
Aortopulmonary window
Cervical venous hum
Anomalous left coronary artery from the pulmonary artery
Mammary souffle of pregnancy
Bronchial collateral circulation
Intercostal or pulmonary arteriovenous fistula
Murmur Type
Location
Quality
Periodicity
Configuration
Radiation
S1
S2
Pitch
MS
Apex
Rumbling
Diastolic
Mid to late diastolic with presystolic accentuation
—
Loud
Initially normal; later, loud P2 with pulmonary hypertension, ultimately single S2
Low
MR
Apex
Blowing
Systolic
Plateau
Axilla/base of heart
Muffled
Widely split
High
AS
Apex/right upper sternal border
Harsh
Systolic
Crescendo-decrescendo
Carotids
Normal
Delayed aortic valve closure causing narrow split or single S2
High
AR
Right upper sternal border/left third/fourth ICS
Blowing
Diastolic
Decrescendo
Apex
Normal/soft
Soft A2, P2 may be obscured by murmur
TR
Left fourth ICS
Blowing
Diastolic
Plateau
Left sternal border/over xiphoid
Muffled
When TR is due to pulmonary hypertension, P2 is accentuated with delayed split
High
PS
Left second ICS
Blowing
Systolic
Crescendo/decrescendo
—
Normal
Loud P2 with prominent split, which becomes fixed with increasing severity
High
VSD
Left lower sternal border
Harsh
Systolic
Plateau
None
—
Split
High
PDA
Left upper sternal border
Harsh
Continuous
Crescendo-decrescendo with peak around S2
None
Normal
Widely split S2 due to delayed P2
High
MVP
Apex
Blowing
Mid-late systolic
Plateau
Axilla/base
Diastolic click
After S1
—
High
HOCM
Left lower sternal border
Harsh
Mid-late systolic
Similar to valvular AS murmur
None
Normal
Normal initially, with increased severity; S2 paradoxically split
High
Ashvarya Mangla, MBBS, MD Adult Hospitalist Services, OSF Saint Francis Medical Center; Clinical Assistant Professor of Medicine, University of Illinois College of Medicine at Peoria
Ashvarya Mangla, MBBS, MD is a member of the following medical societies: American College of Physicians, American Heart Association
Disclosure: Nothing to disclose.
Saurabh Gupta, MD, FACC, FSCAI Director of Structural Cardiology, Heart and Lung Center, St Charles Hospital
Saurabh Gupta, MD, FACC, FSCAI is a member of the following medical societies: American College of Cardiology, American Heart Association, Oregon Medical Association, Society for Cardiovascular Angiography and Interventions
Disclosure: Nothing to disclose.
Richard A Lange, MD, MBA President, Texas Tech University Health Sciences Center, Dean, Paul L Foster School of Medicine
Richard A Lange, MD, MBA is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American Heart Association, Association of Subspecialty Professors
Disclosure: Nothing to disclose.
We would like to thank 3M™ Littmann® stethoscopes for providing audios of heart sounds for this article.
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